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Motor Speech Disorders > Disorders Matrix and Other Final Info > Flashcards

Disorders Matrix and Other Final Info Flashcards

1
Q

flaccid dysarthria: etiologies

A
  • ALS
  • myasthenia gravis
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2
Q

flaccid dysarthria: site of lesion

A

lower motor neuron (LMN)
- final common pathway
- motor unit

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3
Q

flaccid dysarthria: type of damage

A
  • posterior fossa
  • peripheral axon
  • myoneural junction
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4
Q

flaccid dysarthria: characteristics

A
  • weakness
  • reflexive, automatic, and voluntary movements
  • atrophy
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5
Q

flaccid dysarthria: oral mech and motor speech results

A

problems with executing the movement

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6
Q

flaccid dysarthria: characteristics of respiration

A
  • mono loudness
  • speaking on inhalation
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7
Q

flaccid dysarthria: characteristics of phonation

A
  • breathiness
  • stridor
  • diplophonia
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8
Q

flaccid dysarthria: characteristics of articulation

A

weak/slurred

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9
Q

flaccid dysarthria: characteristics of resonance

A

hypernasality

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10
Q

flaccid dysarthria: treatment

A
  • strength: isotonic/isometric exercises
  • effortful closure technique
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11
Q

spastic dysarthria: etiologies

A

ALS, CP, MS

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12
Q

spastic dysarthria: site of lesion

A

upper motor neuron (UMN)
- direct and indirect activation pathways (pyramidal and extrapyramidal)

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13
Q

spastic dysarthria: type of damage

A
  • pyramidal
  • extrapyramidal
  • supratentorial
  • posterior fossa
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14
Q

spastic dysarthria: other notable characteristics

A
  • spasticity
  • decreased reflexes initially, then more pronounced
  • Babinski sign
  • Pseudobulbar affect
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15
Q

spastic dysarthria: oral mech and motor speech results

A
  • slow and regular AMRs
  • articulation errors, but decent prosody (general dysarthria)
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16
Q

spastic dysarthria: characteristics of respiration

A
  • mono loudness
  • intermittent breathy/aphonic segments
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17
Q

spastic dysarthria: characteristics of phonation

A
  • strained
  • harshness
  • pitch breaks
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18
Q

spastic dysarthria: characteristics of articulation

A
  • slow and effortful
  • imprecise, long phoneme duration
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19
Q

spastic dysarthria: characteristics of resonance

A

hypernasality

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20
Q

spastic dysarthria: treatment

A
  • sustained phonation with visual feedback
  • reduced rate techniques
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21
Q

ataxic dysarthria: etiologies

A

AT, MS, Friedrich’s ataxia

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22
Q

ataxic dysarthria: site of lesion

A

cerebellum
- cerebellar control circuit

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23
Q

ataxic dysarthria: type of severity

A

posterior fossa

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24
Q

ataxic dysarthria: characteristics

A
  • incoordination
  • reflexive swallow
  • gag
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25
Q

ataxic dysarthria: oral mech and motor speech results

A
  • irregular and slow AMRs
  • movement is uncoordinated
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26
Q

ataxic dysarthria: characteristics of phonation

A
  • loudness variations
  • coarse voice tremors
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27
Q

ataxic dysarthria: characteristics of articulation

A
  • slow rate
  • prolonged phonemes
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28
Q

ataxic dysarthria: treatment

A
  • contrastive production
  • intelligibility drills
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29
Q

hypokinetic dysarthria: etiologies

A

Parkinson’s disease

30
Q

hypokinetic dysarthria: site of lesion

A

basal ganglia control circuit (extrapyramidal)

31
Q

hypokinetic dysarthria: type of damage

A

supratentorial

32
Q

hypokinetic dysarthria: other notable characteristics

A
  • rigidity, reduced range of movement
  • involuntary movement
  • Bradykinesia or Akinesia
33
Q

hypokinetic dysarthria: oral mech and motor speech results

A
  • rapid, “blurred” AMRs
  • issues with control
34
Q

hypokinetic dysarthria: characteristics of respiration

A
  • breathiness
  • mono loudness
35
Q

hypokinetic dysarthria: characteristics of phonation

A

mono pitch

36
Q

hypokinetic dysarthria: characteristics of articulation

A
  • reduced stress
  • inappropriate silences
37
Q

hypokinetic dysarthria: characteristics of resonance

A

hypernasality

38
Q

hypokinetic dysarthria: treatment

A
  • levodopa (pharmalogical treatment)
  • daily speech program
39
Q

hyperkinetic dysarthria: etiologies

A

Huntington’s disease

40
Q

hyperkinetic dysarthria: site of lesion

A

basal ganglia control circuit (extrapyramidal)

41
Q

hyperkinetic dysarthria: type of damage

A

supratentorial

42
Q

hyperkinetic dysarthria: characteristics

A

involuntary movements

43
Q

hyperkinetic dysarthria: oral mech and motor speech results

A

slow and regular AMRs

44
Q

hyperkinetic dysarthria: characteristics of respiration

A
  • audible inspiration
  • sudden forced inspiration/expiration
45
Q

hyperkinetic dysarthria: characteristics of phonation

A
  • strained harshness
  • voice stoppages
46
Q

hyperkinetic dysarthria: characteristics of articulation

A
  • reduced stress
  • increased rate in segments
47
Q

hyperkinetic dysarthria: characteristics of resonance

A

hypernasality

48
Q

hyperkinetic dysarthria: treatment

A
  • controlled exhalation
  • postural adjustments (upright for inspiration, supine for expiration)
  • optimal breath groups
  • Accent Method of Voice Therapy
49
Q

unilateral UMN: etiologies

A
  • stroke
  • neurosurgery
50
Q

unilateral UMN: characteristics

A
  • weakness
  • incoordination
  • spasticity
51
Q

unilateral UMN: site of lesion

A

upper motor neuron
- direct and indirect pathways (pyramidal and extrapyramidal)

52
Q

unilateral UMN: oral mech and motor speech results

A
  • irregular AMRs
  • velar implications
53
Q

unilateral UMN: characteristics of phonation

A
  • slow rate
  • mono loudness
54
Q

unilateral UMN: characteristics of articulation

A

imprecise, irregular articulatory breakdowns

55
Q

unilateral UMN: treatment

A
  • expiratory muscle strength training
  • phonetic placement
56
Q

mixed dysarthria: etiologies for flaccid-spastic

A

ALS

57
Q

mixed dysarthria: etiologies for spastic-ataxic

A

MS

58
Q

mixed dysarthria: degenerative etiologies

A

ALS, MS, PSP

59
Q

mixed dysarthria: toxic metabolic etiologies

A

Wilson’s disease, Hepatocerebral degeneration, Hypoxic encephalopathy

60
Q

mixed dysarthria: site of lesion

A
  • cerebellum/cerebellar connections
  • UMN
  • LMN
61
Q

mixed dysarthria: treatment

A
  • adjusting posture for breath support
  • visual feedback for articulation
  • emphasizing differences between similar phonemes
  • pacing strategies
  • group phrasing
62
Q

acquired apraxia of speech (AOS): etiologies

A
  • stroke
  • Broca’s aphasia
63
Q

acquired apraxia of speech (AOS): site of lesion

A

left (dominant) hemisphere

64
Q

acquired apraxia of speech (AOS): oral mech and motor speech results

A
  • rapid, “blurred” AMRs
  • poorly sequenced SMRs
65
Q

acquired apraxia of speech (AOS): characteristics of phonation

A
  • mono pitch
  • mono loudness
66
Q

acquired apraxia of speech (AOS): characteristics of articulation

A
  • marked deterioration with increased rate
  • articulatory groping
67
Q

acquired apraxia of speech (AOS): treatment

A
  • articulatory-kinematic
  • melodic intonation therapy (MIT)
  • script training
  • sensory cueing
68
Q

A 55-year-old right-handed man was admitted to the hospital with a 4-day history of progressive right hemiparesis and dysarthria. Neurologic evaluation revealed dysarthria, right hemiparesis, and mild sensory loss in the right face and upper limb. A CT scan showed evidence of an infarct in the posterior limb of the left capsule. Speech evaluation 2 1/2 weeks after onset revealed a right central facial weakness. Speech was characterized by imprecise articulation, harsh voice quality, and slow speech AMRs. Intelligibility was moderately reduced. There was no evidence of aphasia or cognitive disturbance.

A

unilateral upper motor neuron (UUMN) dysarthria

69
Q

A 29-year-old woman presented to a rehabilitation unit 14 months after cerebral anoxia that developed secondary to cardiac arrest during a tubal ligation. Neurologic exam revealed neck and left upper extremity rigidity, and weakness in all extremities. Gait was slow with short steps. She had difficulty with chewing and swallowing and frequently choked on solid foods. Speech evaluation revealed reduced loudness, imprecise articulation, accelerated speech rate, little variation in pitch, loudness and syllable duration, and reduced range of articulatory movement. Speech AMRs were “super fast and blurred.”

A

hypokinetic dysarthria

70
Q

A 63-year-old woman was hospitalized for evaluation/treatment of cardiovascular problems. She had a h/o myocardial infarction and had coronary bypass surgery 6 mo. previously. Three weeks before admission, she developed sudden onset of speech difficulty and problems with gait. She had no difficulties with language, chewing, or swallowing. Oral mechanism exam was normal. Speech was characterized by irregular articulatory breakdowns, irregular speech AMRs, and unsteady vowel prolongation; intelligibility was normal.

A

ataxic dysarthria

Motor Speech Disorders (2 decks)

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